Metabolic heterogeneity of eosinophils from normal and hypereosinophilic patients

Abstract

Eosinophils, which may be associated with allergic, parasitic, or neoplastic disease, have a potent oxidative burst that may be activated by particulate or soluble stimuli. Eosinophils from normal persons and patients with hypereosinophilia were compared with respect to their ability to produce the active oxygen product, superoxide anion. Normal eosinophils produced large amounts of superoxide anion under resting conditions (0.53 +/- 0.15 nmoles cyto-c/10(5) eos/hr) and when stimulated by preopsonized zymosan (0.85 +/0 1.10 nmoles cyto-c/10(5) eos/hr) or phorbol myristate acetate (PMA) (2.38 +/- 0.46 nmoles cyto- c/10(5) eos/hr). Considerable variation was observed in superoxide production by eosinophils from patients with hypereosinophilia. Eosinophils from a group of four patients with hypereosinophilia associated with neoplastic disease produced less superoxide anion than normal eosinophils when stimulated by preopsonized zymosan or PMA (p less than or equal to 0.05). Eosinophils from a group of 5 patients with other causes of hypereosinophilia produced more superoxide anion than normal eosinophils when stimulated by PMA (p less than or equal to 0.01). These studies demonstrate metabolic heterogeneity of eosinophils from patients with hypereosinophilia, and further emphasize that normal eosinophils and eosinophils from hypereosinophilic patients are not functionally equivalent.

Evaluation of myeloid cells (tumor-associated tissue eosinophils and mast cells) infiltration in different grades of oral squamous cell carcinoma

“…Confirmatory evidence has been sporadic, and it is likely that several causes are responsible. [ 65 66 ] Regardless of the cause of accumulation or the mechanism by which eosinophils traffic to tumors, a salient question remains: What are the consequences of this eosinophil infiltration? Specially, are eosinophils destructive, cytotoxic effector cells limiting tumor growth as part of a host surveillance mechanism, or do the infiltrating eosinophils facilitate tumor growth by remodeling and immunoregulation of the tumor microenvironment?…”

Modulation of cell adhesion molecules on human endothelial cells by eosinophil-derived mediators

“…These results suggest that eosinophils but not neutrophils from patients with blood eosinophilia can secrete mediators able to activate endothelial cells, particularly through expression of ICAM-1, E-selectin, and VCAM-1. In our conditions, these eosinophil-derived mediators were spontaneously secreted and several mechanisms may be implicated in the high levels of eosinophilic mediators recovered after 18 h of culture: (1) a protein synthesis; (2) the continuation of eosinophil degranulation as showed by the high increase in ECP levels after 18 h of incubation compared with 1 h; (3) the in vivo priming of these eosinophils due to related pathological situations [2,[26][27][28]. All patients had considerably elevated levels of ECP (128 Ϯ 15 µg/L; expected values are 2-16 µg/L) and soluble IL-2-receptor (3,269 Ϯ 601 pg/mL; expected values are 500 to 2,250 pg/mL) in sera, two factors indicating eosinophil in vivo priming and eosinophilia [29,30].…”

Influence of allergen avoidance at high altitude on serum markers of eosinophil activation in children with allergic asthma

“…A variety of circumstantial evidence suggests that eosinophil leucocytes are intimately involved in the infiammatory process in the bronchial mueosa of asthmatic patients [1.2]. During an asthmatic attack eosinophils are found both in bronehial walls and in airway lumen and they may exert tissue damage by oxygen-dependent as well as oxygen-independent mechanisms [3]. The former is based on the toxic oxygen metabolites and eosinophil peroxidase (EPO) and the latter on granule proteins such as eosinophil eationic protein (ECP), eosinophil peroxidase (EPO), eosinophil protein X/eosinophil derived neurotoxin (EPX/EDN) and major basic protein (MBP).…”